A test meal containing phenol red and hypertonic sucrose was instilled intragastrically into rats through a rubber catheter. The phenol red was used to calculate the volume of gastric contents and the amount of HCl lost from the stomach and, therefore, the quantity of HCl secreted. The stimulating effect of subcutaneous histamine on gastric HCl secretion was studied. Maximum stimulation occurred with doses of more than 2 mg of histamine phosphate. The duration of the response was 45 minutes. Doses of up to 8 mg of histamine phosphate did not produce toxic effects. A 45-minute test meal, in conjunction with a maximum stimulating dose of histamine, was used to demonstrate inhibition of acid secretion and gastric motility following topical application of p-chloromercuribenzoate to the gastric mucosa.

No abstract

Reports of animal experiments and results of preliminary studies by Bean and Hodges (1) in man indicated that the metabolic effects of pantothenic acid deficiency in human subjects would be widespread and profound. Such was the case (2). Insofar as it was possible to predict the metabolic changes in this experiment it seemed likely that one feature would be a suppression of adrenal cortical function and that this might lead to a secondary reduction of gastric secretion. On the other hand, following Lipmann's (3) demonstration that pantothenic acid is the active principle of coenzyme A, it has been shown that many metabolic processes involve acetylation reactions in which coenzyme A is essential (4). This led to the hypothesis that coenzyme A might play a fundamental part in the metabolism of parietal cells and that pantothenic acid deficiency would, therefore, have a direct inhibitory effect on their production of hydrochloric acid. These were the theoretical considerations which led to the special study of gastric function during pantothenic acid deficiency in the hope of obtaining information of physiological and possibly therapeutic interest. This paper reports the results of these studies which were undertaken concurrently with those reported by Bean, Hodges, and Daum (2). MATERIALS AND METHODSThe subjects of the experiment were three normal young adult men who had no previous history of gastrointestinal disease. During the experiment there were five different dietary periods. Since a palatable diet deficient in pantothenic acid cannot be prepared from natural foods, a synthetic liquid formula was prepared and this was administered directly into the stomach through a plastic tube 5 mm. in diameter. This formula, which contained an adequate supply of all essential food factors, including pantothenic acid, was given for an initial control period of 12 days. For a second period of 25 days the same formula was used but pantothenic acid was omitted and omega-methylpantothenic acid, a metabolic antagonist to pantothenic acid, was substituted.In the third phase of the experiment both pantothenic acid and the antagonist were administered with the object of correcting the deficiency. After six days of this regimen the expected improvement in the manifestations of deficiency had not occurred and it became necessary to allow a general diet by mouth supplemented by pantothenic acid and other vitamins. At this stage there were manifestations of insufficiency of the adrenal cortex and cortisone was administered in small daily doses for four days (2). Three days after terminating cortisone therapy tube feeding was resumed and continued for nine days as a final control period. The original formula containing pantothenic acid, but not the antagonist, was administered during this final period.Three tests were selected to compare gastric secretory and motor function during the development of deficiency with the normal function during the initial control period and during the final recovery period. These tests were a modificati...

xiv+ 387; illustrated. £5 4s.) Springfield, Ill.: Charles C Thomas. Oxford: Blackwell Scientific Publications. 1959. This book is based on a programme of lectures and symposia held in the University of California in December 1958, for the purpose of "advancing basic knowledge in the field of gastrointestinal motility". Although the book does not achieve this ambitious aim, it succeeds in giving a stimulating account of some gastrointestinal disorders in terms of disordered motility. There are many distinguished names amongst the 29 contributors,

No abstract